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Activation of human immunodeficiency virus by herpes simplex virus
M P Golden1, S Kim, S M Hammer
1Division of Infectious Diseases, New England Deaconess Hospital, Boston, MA 02215.
The Journal of Infectious Diseases
|September 1, 1992
Summary
Herpes simplex virus (HSV) can reactivate latent human immunodeficiency virus (HIV) in infected cells. Specific HSV proteins, ICP0 and ICP27, are key to this HIV reactivation process.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Heterologous viruses can influence the course of human immunodeficiency virus (HIV) infection.
- Persistent HIV infection in ACH-2 cells provides a model for studying viral interactions.
Purpose of the Study:
- To investigate the role of herpes simplex virus (HSV) type 1 in augmenting HIV type 1 replication.
- To identify specific HSV-1 proteins involved in the reactivation of latent HIV.
Main Methods:
- Superinfection of HIV-1 persistently infected ACH-2 cells with HSV-1.
- Utilized HSV-1 mutants lacking immediate-early genes (ICP0, ICP4, ICP27).
- Northern blot analysis to assess HIV-1 mRNA levels and transcriptional phase.
Main Results:
- HSV-1 superinfection significantly increased HIV-1 replication in ACH-2 cells.
- HSV-1 immediate-early proteins ICP0 and ICP27, but not ICP4, were essential for up-regulating HIV replication.
- Activation of HIV was characterized by a shift in mRNA levels, mimicking early-to-late transition.
Conclusions:
- HSV can activate HIV-1 from latency in ACH-2 cells.
- This activation is independent of productive HSV replication.
- The process involves increased steady-state levels of HIV transcripts, mediated by specific HSV proteins.